Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation studies were performed in a patient who had been bitten by a snake of the species Bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. Fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. In vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate Factor XIII. In vivo consumption of Factor XIII after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.
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PMID:Coagulopathy after snake bite by Bothrops neuwiedi: case report and results of in vitro experiments. 229 86

Asphyxiated newborns have evidence of disseminated intravascular coagulation (DIC). Several hemostatic parameters were assayed in venous umbilical cord blood of 93 infants, 58 of which suffered from asphyxia due to abruptio placentae, breech delivery, preeclampsia, dead twin, and amniotic fluid embolism. Levels of factor XIII were markedly lower in the high-risk infants; the lowest values coincided with lowest Apgar scores. Plasma levels of thrombin-antithrombin (TAT) complexes, D-dimer, fibrin(ogen) degradation products (FDP), and soluble fibrin monomer complexes (SFMC) were markedly higher in the asphyxiated newborns with good correlations to DIC scores. DIC scores for infants were explained. A significant negative correlation was found between plasma levels of SFMC and Apgar scores. Also primary hemostasis measurements by a Thrombostat 4000 revealed defects in the asphyxiated infants. The data strongly suggest the presence of DIC in the high-risk group of infants.
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PMID:Hypercoagulability and DIC in high-risk infants. 983 14